Social and Genetic Pathways in Multigenerational Transmission of Educational Attainment

2018 ◽  
Vol 83 (2) ◽  
pp. 278-304 ◽  
Author(s):  
Hexuan Liu

This study investigates the complex roles of the social environment and genes in the multigenerational transmission of educational attainment. Drawing on genome-wide data and educational attainment measures from the Framingham Heart Study (FHS) and the Health and Retirement Study (HRS), I conduct polygenic score analyses to examine genetic confounding in the estimation of parents’ and grandparents’ influences on their children’s and grandchildren’s educational attainment. I also examine social genetic effects (i.e., genetic effects that operate through the social environment) in the transmission of educational attainment across three generations. Two-generation analyses produce three important findings. First, about one-fifth of the parent-child association in education reflects genetic inheritance. Second, up to half of the association between parents’ polygenic scores and children’s education is mediated by parents’ education. Third, about one-third of the association between children’s polygenic scores and their educational attainment is attributable to parents’ genotypes and education. Three-generation analyses suggest that genetic confounding on the estimate of the direct effect of grandparents’ education on grandchildren’s education (net of parents’ education) may be inconsequential, and I find no evidence that grandparents’ genotypes significantly influence grandchildren’s education through non-biological pathways. The three-generation results are suggestive, and the results may change when different samples are used.

2019 ◽  
Vol 28 (1) ◽  
pp. 82-90 ◽  
Author(s):  
Daniel W. Belsky ◽  
K. Paige Harden

Genome-wide association studies (GWASs) have identified specific genetic variants associated with complex human traits and behaviors, such as educational attainment, mental disorders, and personality. However, small effect sizes for individual variants, uncertainty regarding the biological function of discovered genotypes, and potential “outside-the-skin” environmental mechanisms leave a translational gulf between GWAS results and scientific understanding that will improve human health and well-being. We propose a set of social, behavioral, and brain-science research activities that map discovered genotypes to neural, developmental, and social mechanisms and call this research program phenotypic annotation. Phenotypic annotation involves (a) elaborating the nomological network surrounding discovered genotypes, (b) shifting focus from individual genes to whole genomes, and (c) testing how discovered genotypes affect life-span development. Phenotypic-annotation research is already advancing the understanding of GWAS discoveries for educational attainment and schizophrenia. We review examples and discuss methodological considerations for psychologists taking up the phenotypic-annotation approach.


2018 ◽  
Vol 83 (4) ◽  
pp. 802-832 ◽  
Author(s):  
Robbee Wedow ◽  
Meghan Zacher ◽  
Brooke M. Huibregtse ◽  
Kathleen Mullan Harris ◽  
Benjamin W. Domingue ◽  
...  

Sociologists interested in the effects of genes on complex social outcomes claim environmental conditions structure when and how genes matter, but they have only studied environmental moderation of genetic effects on single traits at a time (gene-by-environment interactions). In this article, we propose that the social environment can also transform the genetic link between two traits. Taking the relationship between educational attainment and smoking as an exemplary case, we use genome-wide methods to examine whether genetic variants linked to education are also linked to smoking, and whether the strength of this relationship varies across birth cohorts. Results suggest that the genetic relationship between education and smoking is stronger among U.S. adults born between 1974 and 1983 than among those born between 1920 and 1959. These results are supported by replication in additional data from the United Kingdom. Environmental conditions that differ across birth cohorts may result in the bundling of genetic effects on multiple outcomes, as anticipated by classic cohort theory. We introduce genetic correlation-by-environment interaction [(rG)xE] as a sociologically-informed model that will become especially useful as data for more well-powered analyses become available.


2012 ◽  
Vol 21 (11 Supplement) ◽  
pp. 04-04
Author(s):  
Philip J. Lupo ◽  
Michael E. Scheurer ◽  
Georgina N. Armstrong ◽  
Spiridon Tsavachidis ◽  
Yanhong Liu ◽  
...  

2019 ◽  
Vol 32 (7-8) ◽  
pp. 753-763
Author(s):  
Aniruddha Das

Objectives: Rather than acting as a buffer, educational attainment has a known positive linkage with major experiences of lifetime discrimination. Recently established genetic roots of education, then, may also influence such reports. The current study examined these patterns. Methods: Data were from the 2010 wave of the Health and Retirement Study. Polygenic scores indexed one’s genetic propensity for more education. Mediation analysis was through counterfactual methods. Results: Among Whites as well as Blacks, genetic antecedents of education also elevated discrimination reports. Part of this influence was channeled through education. At least among Whites, direct effects were also found. Discussion: Major discrimination experiences seem partly rooted in genes. Mechanisms are tentatively suggested. Direct genetic influences, in particular, indicate potential confounding of previously estimated linkages between discrimination and health or life course factors. Given the range of these prior results, and their implications for healthy aging, investigation of these possibilities is needed.


2019 ◽  
Author(s):  
Jornt Mandemakers ◽  
Kasper Otten

Abstract‘Social contagion’ research suggests that health behaviors (BMI, smoking, drinking, etc.) spread through social networks, including dyadic ties such as between married/cohabiting partners. However, separating contagion from assortative mating (‘like seeks like’) and shared environmental factors remains notoriously difficult in observational studies. It is not possible to obtain exogenous variation in long-term partnerships (‘random mating’), but genetic approaches can offer a novel way to examine partner similarity and the role of social contagion. This paper explores possible social genetic effects among partners, i.e., effects of the partner’s genes on one’s own behavior. We use the longitudinal Health and Retirement Study with data on health behavior and genomic data for both ego and his/her partner to examine social genetic effects for BMI, drinking, and smoking behavior. For each outcome, we find support for social genetic effects. Americans of European descent were more overweight if they had partners with higher polygenic scores for BMI net of their own polygenic score. Similar findings were found for the number of drinks per week and cigarettes per day. Longitudinal analyses that conditioned on past health behavior of both spouses confirmed these findings. We further explored whether susceptibility to the partner’s influence differed between men and women, but did not find consistent differences across outcomes. Findings are further discussed in the light of ramifications of social genetic effects for the social and biological sciences.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Declan Bennett ◽  
Donal O’Shea ◽  
John Ferguson ◽  
Derek Morris ◽  
Cathal Seoighe

AbstractOngoing increases in the size of human genotype and phenotype collections offer the promise of improved understanding of the genetics of complex diseases. In addition to the biological insights that can be gained from the nature of the variants that contribute to the genetic component of complex trait variability, these data bring forward the prospect of predicting complex traits and the risk of complex genetic diseases from genotype data. Here we show that advances in phenotype prediction can be applied to improve the power of genome-wide association studies. We demonstrate a simple and efficient method to model genetic background effects using polygenic scores derived from SNPs that are not on the same chromosome as the target SNP. Using simulated and real data we found that this can result in a substantial increase in the number of variants passing genome-wide significance thresholds. This increase in power to detect trait-associated variants also translates into an increase in the accuracy with which the resulting polygenic score predicts the phenotype from genotype data. Our results suggest that advances in methods for phenotype prediction can be exploited to improve the control of background genetic effects, leading to more accurate GWAS results and further improvements in phenotype prediction.


2016 ◽  
Author(s):  
BENJAMIN W DOMINGUE ◽  
Jason D. Boardman

We use genome-wide data from the third generation respondents of the Framingham Heart Study to estimate heritability in body mass index using different quantities of the measured genotype. Heritability decreases rapidly when SNPs implicated by a genome-wide association study are removed but shows essentially no decline when SNPs implicated by a gene-environment interaction in a second genome-wide analysis are removed. This second result is highlighted by our additional finding that the SNPs which explain heritability amongst a subsample defined by higher educational attainment explain no heritability of the heritability in the lower education group, and vice-versa. Finally, we do find consistent heritability estimates when we compare family-based estimates versus those based on measured genotype.


2021 ◽  
pp. 1-11
Author(s):  
Jeremy Harper ◽  
Mengzhen Liu ◽  
Stephen M. Malone ◽  
Matt McGue ◽  
William G. Iacono ◽  
...  

Abstract Background To better characterize brain-based mechanisms of polygenic liability for psychopathology and psychological traits, we extended our previous report (Liu et al. Psychophysiological endophenotypes to characterize mechanisms of known schizophrenia genetic loci. Psychological Medicine, 2017), focused solely on schizophrenia, to test the association between multivariate psychophysiological candidate endophenotypes (including novel measures of θ/δ oscillatory activity) and a range of polygenic scores (PGSs), namely alcohol/cannabis/nicotine use, an updated schizophrenia PGS (containing 52 more genome-wide significant loci than the PGS used in our previous report) and educational attainment. Method A large community-based twin/family sample (N = 4893) was genome-wide genotyped and imputed. PGSs were constructed for alcohol use, regular smoking initiation, lifetime cannabis use, schizophrenia, and educational attainment. Eleven endophenotypes were assessed: visual oddball task event-related electroencephalogram (EEG) measures (target-related parietal P3 amplitude, frontal θ, and parietal δ energy/inter-trial phase clustering), band-limited resting-state EEG power, antisaccade error rate. Principal component analysis exploited covariation among endophenotypes to extract a smaller number of meaningful dimensions/components for statistical analysis. Results Endophenotypes were heritable. PGSs showed expected intercorrelations (e.g. schizophrenia PGS correlated positively with alcohol/nicotine/cannabis PGSs). Schizophrenia PGS was negatively associated with an event-related P3/δ component [β = −0.032, nonparametric bootstrap 95% confidence interval (CI) −0.059 to −0.003]. A prefrontal control component (event-related θ/antisaccade errors) was negatively associated with alcohol (β = −0.034, 95% CI −0.063 to −0.006) and regular smoking PGSs (β = −0.032, 95% CI −0.061 to −0.005) and positively associated with educational attainment PGS (β = 0.031, 95% CI 0.003–0.058). Conclusions Evidence suggests that multivariate endophenotypes of decision-making (P3/δ) and cognitive/attentional control (θ/antisaccade error) relate to alcohol/nicotine, schizophrenia, and educational attainment PGSs and represent promising targets for future research.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 342-342
Author(s):  
Yang Li ◽  
Jan Mutchler ◽  
Edward Miller ◽  
Jing Jian Xiao ◽  
Reginald Tucker-Seeley

Abstract Despite a large body of literature documenting the association between individual characteristics and financial literacy, our understanding of the impact of macro-environmental conditions on individual financial literacy remains limited, particularly in later life. Drawing from a micro-macro perspective on the social environment and individual processes, we examined the extent to which three state-level contextual characteristics were associated with individual later-life financial literacy in the United States: tertiary educational attainment, poverty prevalence, and Internet penetration. We utilized data from the 2019 Understanding America Study (UAS) for adults aged 50 years or older to assess financial literacy (n=2,930), and data from the American Community Survey to evaluate contextual conditions. The UAS is a nationally representative survey panel supported by the Social Security Administration and the National Institute on Aging. Cross-sectional multilevel regression models were used to examine the hypothesized effects. We found that state-level poverty prevalence was negatively associated with individual financial literacy while state-level Internet penetration was positively associated with individual financial literacy, over and above individual characteristics known to impact financial literacy. No association was found between state-level educational attainment and individual financial literacy after controlling for respondents’ own education. Findings suggest that the social environment may condition financial literacy in later life through exposure to opportunities that promote knowledge acquisition. Interventions to enhance later-life financial literacy may benefit from targeted approaches that take into account the environmental characteristics of their locations of residence.


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